Sleep Apnea Tied to Lower Risk of Cardiac Event Recurrence

Decade-long study upends conventional wisdom

SEATTLE -- Individuals in a long-running cohort study with coronary heart disease who also had sleep apnea showed lower rates of recurrent cardiac events than otherwise similar participants without sleep apnea, researchers said here.

After adjusting for nearly a dozen potential confounders, the participants with sleep apnea were at 21% lower risk of recurrent events, defined as myocardial infarction or revascularizations (hazard ratio 0.79, 95% CI 0.65-0.97, per 10-point increase in baseline apnea/hypopnea index [AHI] value), with median 9.0 years of follow-up after enrollment, according to Neomi Shah, MD, MPH, of Montefiore Medical Center and Albert Einstein College of Medicine in the Bronx, N.Y.

At last follow-up, which extended to more than 4,000 days, about 20% of those with AHI values greater than 30 had experienced a recurrent event, compared with about 35% to 40% of those with lower AHI values, Shah and colleagues reported in a poster presented at SLEEP 2015, the annual meeting of the Associated Professional Sleep Societies.

There also appeared to be a sort of dose-response relationship, the researchers found: higher AHI values appeared to correspond to progressively lower risk of recurrent cardiac events. Those with baseline AHI values of 5 to 14.9 showed hazard ratio of 0.80 with participants with AHI <5 (interpreted as no sleep apnea), whereas the hazard ratio for those with AHI values ≥30 was 0.43 compared with the no-apnea group. Although these between-group comparisons did not reach statistical significance, the overall trend per 10-point increase in AHI was significant at P=0.024.

In terms of raw numbers, 57 of 187 participants without apnea at baseline experienced events versus 6 of 31 of those with AHI values ≥30.

Sleep apnea has been associated with a host of adverse outcomes, ranging from increased risk of primary cardiovascular events (including in a previous study by Shah) and dementia to early mortality. Thus, the association with reduced risk of recurrent coronary events was surprising.

The statistical analyses were adjusted for age, sex, body mass index, smoking status, total and HDL cholesterol, diabetes mellitus, systolic and diastolic blood pressure, and use of lipid-lowering and antihypertensive medications.

Results adjusted only for the first four of those variables were virtually identical to those including adjustments for all 11.

The findings came from the Sleep Heart Health Study, which comprises 6,441 participants from seven pre-existing cohorts enrolled and examined from 1995 to 1998. Of these, 440 had histories of myocardial infarction or revascularizations at enrollment and were the sample analyzed in the current study.

Sleep apnea was determined at baseline, on the basis of AHI values obtained via polysomnography, in which only apnea/hypopnea episodes leading to at least 4% drops in oxygen saturation were counted. Participants were stratified according to AHI values below 5 (n=187), 5-14.9 (n=146), 15-29.9 (n=76), and ≥30 (n=31). The parent cohorts (which were administered separately and had their own procedures for detecting events) supplied data on recurrent events.

Mean age for included participants was 70 at enrollment (SD 10) and mean BMI was 27.8. Overall, recurrent MI was seen in 15.5% of participants; a total of 29.6% experienced either recurrent MI or recurrent revascularization.

Kaplan-Meier curves for the accumulation of events during follow-up, stratified into the four AHI tiers, showed almost perfectly linear declines over time, with separation between the highest AHI tier and the other three evident within the first 3 years.

However, Shah and colleagues noted that survival bias was an important limitation of the study. They also refrained from suggesting that sleep apnea was actively, causally protective.

"Further work is required to replicate and further characterize the ... association," they indicated.

But David Rapoport, MD, of the NYU Sleep Medicine Center in New York City, who was not involved with the study, told MedPage Today that it's conceivable that the findings do actually reflect a causal relationship.

He noted that animal and some limited human data have shown that brief exposures to intermittent hypoxia -- like that occurring with sleep apnea -- induce a protective reaction against later, more severe hypoxic episodes, such as in cardiac surgery.

"The presumed lesson from this is the repetitive hypoxia may induce factors that are then protective and mitigate or compensate for the risk of something we assume is 'bad,' i.e., intermittent hypoxia," he said. However, Rapoport cautioned that this is an "intriguing but unproven hypothesis" in the context of sleep apnea.

The study was funded by the National Heart, Lung and Blood Institute. Authors declared no relevant financial interests.

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